Im on HCG and all I can tell you is they will never increase more than what you had before. If you're also taking testosterone youre not getting any more LH. HCG mimics LH in the testicles. It can and usually does reverse atrophy. It will also add more E2 so its a tradeoff.
Cant answer the water question other then to say HCG can increase water retention.
Cant answer the water question other then to say HCG can increase water retention.
Rock H. Johnson
Active Member
HCG or LH also enters the testes, stimulating the interstitial cells, called Leydig cells, to make and release testosterone into the testes and the blood. This inter testicular testosterone, stimulates spermatogenesis, or the process of sperm production in the testes. This contributes often to the 30% size decrease after Exogenous Testosterone shut down the HPG and following loss of semen production.
I know there is much more to it but if someone wants to improve or correct this, be my guest.
Last edited:
madman
Super Moderator
LH stimulates the Leydig cells in the testes to produce ITT (intratesticular testosterone) and ITT/FSH stimulates the Sertoli/germ cells located inside the seminiferous tubule lobes to produce sperm.
When one uses exogenous testosterone/AAS it results in shut down of the HPG axis and the pituitary no longer secretes LH/FSH.
Lack of LH causes atrophy of the Leydig cells which are located between the seminiferous tubules and lack of ITT/FSH causes atrophy of the Sertoli/germ cells which are located inside the seminiferous tubules. The cells shrink and become dormant.
The body no longer produces endogenous testosterone and sperm production is halted.
The Leydig cells only make up 10-20% of testicular volume as oppose to the germ cells/seminiferous tubules (where sperm is produced) which make up almost 80% of the testicular volume so a majority of the shrinkage results from atrophy of the germ cells/seminiferous tubules.
Basically comes down to exogenous testosterone use results in significant suppression of spermatogenesis which leads to testicular shrinkage as a majority of teste volume is made up of germ cells located in the tightly bundled seminiferous tubule lobes where sperm is produced.
Not only does FSH stimulate sperm production but ITT alone is also playing a strong role.
Regarding the use of hCG we can take it along with trt to maintain fertility/prevent testicular shrinkage.
The use of hCG will mimic LH and result in stimulating the Leydig cells in the testes to produce ITT which will have a big impact on stimulating the Sertoli/germ cells located inside the seminiferous tubule lobes to produce sperm and this will cause an increase in testicular volume.
The use of Clomid stimulates LH and FSH which will increase testosterone/sperm production and maintain testicular size.
Vince
Super Moderator
When to add HCG to TRT?
I'm currently on Testosterone Cypionate only, and have been for about four months. I'm still not feeling 100%, but I have been making small adjustments every 2 months or so. I'm trying to get HCG as well, and have been fighting my doctor to get it. I keep asking myself this question, should I...
www.excelmale.com
Vince
Super Moderator
POLL about add hcg
Hi to everybody: How many people here: USE, and FEEL BETTER adding HCG on TRT (and if possible also explain why: how or what feel better)? Thank you .
www.excelmale.com
Vince
Super Moderator
What is the best dose of HCG? Dr Saya presents two case studies.
Community - I am sharing and have attached the write-up of a recent small case study I have conducted on quantitative serum beta hCG concentrations relating to hCG injections. This study is limited to dosages of 150iu and 500iu, although I hope to obtain more data in the near future. P.S...
www.excelmale.com
madman
Super Moderator
Food for thought!
The bulk of the volume of the testis is filled with the seminiferous tubules: There may be several hundred to a thousand or so per testis. Each one consists of a long loop whose outlet is via channels in the tunica albuginea.
The bulk of the testicular tissue is the seminiferous tubules which are present in astonishing quantity. A human testis may have 800-1600 tubules, with an aggregated length of about 600 meters: that's a shade over 1950 feet, which is a good deal longer than the Empire State Building is high.
The bulk of the volume of the testis is filled with the seminiferous tubules: There may be several hundred to a thousand or so per testis. Each one consists of a long loop whose outlet is via channels in the tunica albuginea.
The bulk of the testicular tissue is the seminiferous tubules which are present in astonishing quantity. A human testis may have 800-1600 tubules, with an aggregated length of about 600 meters: that's a shade over 1950 feet, which is a good deal longer than the Empire State Building is high.
Last edited:
Does anyone know what compounds the body uses to create the extra size increase? Is it just water that is absorbed by activation in the once dormant cells?
madman
Super Moderator
Again a majority of teste volume is made up of seminiferous tubules where sperm production takes place.
The tubules are lined with a germinal epithelium which is the wall of the seminiferous tubules made up of numerous (Sertoli/germ cells) which produce sperm.
The bulk of the seminiferous tubule lobes are Sertoli/germ cells (immature sperm) which develop into mature sperm.
Germinal epithelium (male) - Wikipedia
en.wikipedia.org
The germinal epithelium is the epithelial layer of the seminiferous tubules of the testicles. It is also known as the wall of the seminiferous tubules. The cells in the epithelium are connected via tight junctions.
There are two types of cells in the germinal epithelium. The large Sertoli cells (which are not dividing) function as supportive cells to the developing sperm. The second cell type are the cells belonging to the spermatogenic cell lineage. These develop to eventually become sperm cells (spermatozoon). Typically, the spermatogenic cells will make four to eight layers in the germinal epithelium.[1]
Identifiers |
|---|
Germinal epithelium of the testicle. 1 basal lamina, 2 spermatogonia, 3 spermatocyte 1st order, 4 spermatocyte 2nd order, 5 spermatid, 6 mature spermatid, 7 Sertoli cell, 8 tight junction (blood testis barrier) |
Does anyone know what compounds the body uses to create the extra size increase?
Refer to sections underlined/highlighted in red.
Important points to keep in mind:
*Sertoli cells synthesize and secrete a large variety of factors: proteins, cytokines, growth factors, opioids, steroids, prostaglandins, modulators of cell division etc. The morphology of Sertoli cells is strictly related to their various physiological functions. Cytoplasm contains endoplasmic reticulum both of the smooth (steroid synthesis) and rough type (protein synthesis), a prominent Golgi apparatus (elaboration and transport of secretory products), lysosomal granules (phagocytosis) as well as microtubuli and intermediate filaments (adapation of the cell shape during the different phases of germ cell maturation).
*Another important function of Sertoli cells is that they are responsible for final testicular volume and sperm production in the adult. Each individual Sertoli cell is in morphological and functional contact with a defined number of sperm.
*Through the production and secretion of tubular fluid Sertoli cells create and maintain the patency of the tubulus lumen. More than 90% of Sertoli cell fluid is secreted in the tubular lumen.
*Sperm are transported in the tubular fluid, the composition of which is known in detail only in the rat (Setchell 1999). Unlike blood, the tubular fluid contains a higher concentration of potassium ions and a lower concentration of sodium ions. Other constituents are bicarbonate, magnesium and chloride ions, inositol, glucose, carnitine, glycerophosphorylcholine, amino acids and several proteins. Therefore, the germ cells are immersed in a fluid of unique composition.
Nieschlag
Leydig Cells
Leydig cells are rich in smooth endoplasmic reticulum and mitochondria with tubular cristae.
Other important cytoplasmic components are lipofuscin granules, the final product of endocytosis and lyosomal degradation, and lipid droplets, in which the preliminary stages of testosterone synthesis take place. Special formations, called Reinke’s crystals, are often found in the adult Leydig cells. These are probably subunits of globular proteins whose functional meaning is not known.
Peritubular Cells
The seminiferous tubules are covered by a lamina propria, which consists of a basal membrane, a layer of collagen and the peritubular cells (myofi broblasts). These cells are stratified around the tubulus and form up to concentrical layers that are separated by collagen layers.
Peritubular cells produce several factors that are involved in cellular contractility: panactin, desmin, gelsolin, smooth muscle myosin and actin (Holstein et al. 1996). These cells also secrete extracellular matrix and factors typically expressed by connective tissue cells: collagen, laminin, vimentin, fibronectin, growth factors, fibroblast protein and adhesion molecules.
Sertoli Cells
Sertoli cells are somatic cells located within the germinal epithelium.
These cells are located on the basal membrane and extend to the lumen of the tubulus seminiferus and, in a broad sense, can be considered as the supporting structure of the germinal epithelium. Along the cell body, extending over the entire height of the germinal epithelium, all morphological and physiological differentiation and maturation of the germinal cell up to the mature sperm take place. Special ectoplasmic structures sustain alignment and orientation of the sperm during differentiation. About 35–40% of the volume of the germinal epithelium is represented by Sertoli cells.
Sertoli cells synthesize and secrete a large variety of factors: proteins, cytokines, growth factors, opioids, steroids, prostaglandins, modulators of cell division etc. The morphology of Sertoli cells is strictly related to their various physiological functions. Cytoplasm contains endoplasmic reticulum both of the smooth (steroid synthesis) and rough type (protein synthesis), a prominent Golgi apparatus (elaboration and transport of secretory products), lysosomal granules (phagocytosis) as well as microtubuli and intermediate filaments (adapation of the cell shape during the different phases of germ cell maturation). It is generally assumed that Sertoli cells coordinate the spermatogenic process topographically and functionally. On the other hand, more recent data support the contention that germ cells control Sertoli cell functions.
Another important function of Sertoli cells is that they are responsible for final testicular volume and sperm production in the adult. Each individual Sertoli cell is in morphological and functional contact with a defined number of sperm. The number of sperm per Sertoli cell depends on the species. In men we observe about 10 germ cells or 1.5 spermatozoa per each Sertoli cell (Zhengwei et al. 1998a). In comparison, every macaque monkey Sertoli cell is associated with 22 germ cells and 2.7 sperm (Zhengwei et al. 1997, 1998b). This suggests that within a certain species a higher number of Sertoli cells results in a greater production of sperm and testis size, assuming that all the Sertoli cells are functioning normally. In contrast, as determined by flow cytometry, testicular cell numbers were very similar across several primate species, suggesting that testis size is the main determinant of total germ cell output (Luetjens et al. 2005).
Through the production and secretion of tubular fluid Sertoli cells create and maintain the patency of the tubulus lumen. More than 90% of Sertoli cell fluid is secreted in the tubular lumen. Special structural elements of the blood-testis barrier prevent reabsorption of the secreted fluid, resulting in pressure that maintains the patency of the lumen. Sperm are transported in the tubular fluid, the composition of which is known in detail only in the rat (Setchell 1999). Unlike blood, the tubular fluid contains a higher concentration of potassium ions and a lower concentration of sodium ions. Other constituents are bicarbonate, magnesium and chloride ions, inositol, glucose, carnitine, glycerophosphorylcholine, amino acids and several proteins. Therefore, the germ cells are immersed in a fluid of unique composition.
madman
Super Moderator
Regarding testicular atrophy, as you know the degree to which one would experience such comes down to the individual as some men tend to have minimal shrinkage as opposed to others in which it may be more extreme.
Also if someone naturally has large testis pre-trt then they may not notice the atrophy as much compared to someone who has smaller sized testes.
Although testicular shrinkage is a common side-effect when on trt I would think that the severity would not be too extreme when compared to men using/abusing testosterone/AAS in very high supra-physiological doses.
Let alone many of these same men tend to stack numerous compounds during a cycle which in most cases will result in extreme testicular atrophy.
Fig. 9 Testicular atrophy in a 30-year old AAS abuser (right) compared to normal size (left)
Also if someone naturally has large testis pre-trt then they may not notice the atrophy as much compared to someone who has smaller sized testes.
Although testicular shrinkage is a common side-effect when on trt I would think that the severity would not be too extreme when compared to men using/abusing testosterone/AAS in very high supra-physiological doses.
Let alone many of these same men tend to stack numerous compounds during a cycle which in most cases will result in extreme testicular atrophy.
Fig. 9 Testicular atrophy in a 30-year old AAS abuser (right) compared to normal size (left)
Which works better? Clomid or FSH for testicle growth?
madman
Super Moderator
Regarding preventing/minimizing testicular atrophy if you are currently on trt then adding in hCG using an effective dose should be all you need mind you hCG +FSH would most likely keep the testes volume fuller/larger.
If you are concerned with fertility then hCG + rhFSH may be needed/more effective in some cases.
Testosterone Is a Contraceptive and Should Not Be Used in Men Who Desire Fertility
Amir Shahreza Patel, Joon Yau Leong, Libert Ramos, Ranjith Ramasamy
PHYSIOLOGY OF TESTOSTERONE
In healthy adult men, testosterone production is precisely regulated by the HPG axis. Higher cortical centers in the brain signal the hypothalamus to secrete gonadotropin-releasing hormone (GnRH) in a pulsatile fashion. GnRH in turn stimulates the release of LH and FSH from the anterior pituitary which modulates testosterone production from the Leydig cells and spermatogenesis by the Sertoli cells, respectively. As testosterone levels increase, negative feedback suppression is exerted on the androgen receptors in the hypothalamic neurons and pituitary gland, thereby inhibiting the release of GnRH, FSH, and LH [5].
The exogenous administration of testosterone suppresses the release of gonadotropins (FSH and LH) to levels below that required for spermatogenesis. Spermatogenesis is largely dependent on the action of FSH on Sertoli cells coupled with high intra-testicular testosterone concentrations. Within the seminiferous tubules, only Sertoli cells possess receptors for both FSH and testosterone. Numerous signaling pathways are activated when FSH binds to FSH receptors on these cells. It acts synergistically with testosterone to increase fertility and the efficiency of spermatogenesis [6]. The inhibition of LH release by exogenous testosterone leads to the suppression of endogenous testosterone production by the Leydig cells. The decreased intra-testicular testosterone combined with the suppression of FSH leads to decreased germ cell survival and maturation (Fig. 1).
*Ultimately, the low intra-testicular testosterone results in decreased proliferation of spermatogonia, defects in spermiation of mature spermatozoa by Sertoli cells, and accelerated apoptosis of spermatozoa [8- 11]. Since 80% of testicular volume consists of germinal epithelium and seminiferous tubules, a reduction in these cells is usually manifested by testicular atrophy and this reflects the loss of both spermatogenesis and Leydig cell function [12,13]
*Adjunctive hCG and clomiphene can be used with TRT to maintain testicular size and intra-testicular testosterone concentrations [52].
Indications for the use of human chorionic gonadotropic hormone for the management of infertility in hypogonadal men (2018)
John Alden Lee, Ranjith Ramasamy
Luteinizing hormone (LH) in the male is produced by the anterior pituitary in response to pulsatile secretion of gonadotropic releasing hormone (GnRH) from the hypothalamus. It acts on Leydig cells in the testicles promoting the production of testosterone. In men with hypogonadotropic hypogonadism (HH), or men with decreased LH secondary to exogenous testosterone use, the lack of LH results in severely decreased intratesticular testosterone levels. Without intratesticular testosterone, spermatogenesis is impaired, and by replacing lost LH production with hCG, spermatogenesis can be restored by restoring adequate levels of intratesticular testosterone.
Finally, hCG has also been used to reduce some of the side effects of TRT, mainly preventing testicular atrophy and helping maintain response to TRT by “cycling off” TRT with a periodic replacement of therapy with hCG.
Indications for hCG in combination with TRT
Preserving spermatogenesis with TRT
Exogenous steroid use impairs spermatogenesis by promoting negative feedback on both the hypothalamus and the pituitary gland. This reduces the pulsatile secretion of GnRH and LH respectively. The loss of LH secretion shuts down the production of testosterone by Leydig cells which in turn significantly reduces intratesticular testosterone levels. This altering of the hypothalamus-pituitary-gonadal (HPG) axis and drop of intratesticular testosterone can lead to azoospermia within 10 weeks of starting TRT (10). Even more alarming is the fact that up to 10% of men can remain azoospermic after the cessation of TRT.
hCG therapy can help preserve spermatogenesis in men undergoing TRT by maintaining intratesticular testosterone levels. It was has been shown that follicle-stimulating hormone (FSH) alone cannot initiate or maintain spermatogenesis in hypogonadal (11) men leading to the discovery of the importance of intratesticular testosterone in spermatogenesis. In healthy eugonadal men selected to undergo TRT, it was shown that their intratesticular testosterone levels dropped by 94%. However, in those who received 250 IU SC every other day along with TRT, their intratesticular testosterone levels only dropped 7%. Additionally, men who received TRT and 500 IU of hCG every other day, and an increase in intratesticular testosterone by 26% was observed (12). This proved that co-administering low dose hCG could maintain intratesticular testosterone in those undergoing TRT. It was later shown that not only is intratesticular testosterone increased with co-administration hCG but spermatogenesis is preserved as well at one year follow up (13). These studies proved that by concomitant hCG administration with TRT spermatogenesis and thus potentially fertility could be preserved.
Based on this evidence an algorithm was suggested for the simultaneous treatment of hypogonadism and preservation of fertility (14). All men wishing to preserve fertility while on TRT should have a baseline semen analysis (SA). Next, it is important to determine the appropriate dosing regimen of hCG based on the timeline for the desired pregnancy. For men who wish to obtain pregnancy within six months, it was suggested to discontinue TRT and start 3,000 IU of hCG intramuscular, or subcutaneous every other day. SA should then be performed every two months. Clomiphene citrate 25–50 mg PO daily can be added or omitted to promote FSH production (15). We suggest including of clomiphene citrate in all men who are already oligospermic or azoospermic. It can be omitted in men who are initiating TRT and hCG simultaneously and have normal semen parameters.
If Semen parameters fail to improve and FSH remains low, Gonal-f (recombinant FSH) 75 IU every other day can be added. In men who desire pregnancy within 6–12 months, TRT can be continued with co-administration of 500 IU of HCG every other day ± clomiphene citrate can be used. When planning for pregnancy in greater than 12 months TRT should be cycled off every six months replaced by a four-week cycle of 3,000 IU of hCG every other day. For men who do not desire to preserve fertility testicular size can be maintained while undergoing TRT with 1,500 IU of HCG given weekly. Which is enough to maintain pre-TRT levels of intratesticular testosterone (11). Table 1 summarizes recommendations for preserving spermatogenesis in men on TRT (16).
Nelson Vergel
Founder, ExcelMale.com
Testicular volume in infertile versus fertile white-European men: a case-control investigation in the real-life setting - PubMed
Testicular volume (TV) is considered a good clinical marker of hormonal and spermatogenic function. Accurate reference values for TV measures in infertile and fertile men are lacking. We aimed to assess references values for TV in white-European infertile men and fertile controls. We analyzed...
pubmed.ncbi.nlm.nih.gov
Share this page
Sponsors
Online statistics
- Members online
- 1
- Guests online
- 2
- Total visitors
- 3
